Sirt3 confers protection against acrolein-induced oxidative stress in cochlear nucleus neurons

摘要: Acrolein is a ubiquitous dietary and environmental pollutant, which can also be generated endogenously during cellular stress. However, the molecular mechanisms underlying acrolein-induced neurotoxicity, especially in ototoxicity conditions, have not been fully determined. In this study, we investigated on toxicity primary cultured cochlear nucleus neurons with focus Sirt3, mitochondrial deacetylase. We found that acrolein treatment induced neuronal injury programmed cell death (PCD) dose dependent manner neurons, was accompanied by increased intracellular reactive oxygen species (ROS) generation lipid peroxidation. exposure significantly reduced membrane potential (MMP) levels, promoted cytochrome c release decreased ATP production. addition, ER tracker fluorescence activation of stress factors were observed after treatment, inhibitors shown to attenuate neurons. The results western blot RT-PCR showed markedly expression Sirt3 at both mRNA protein activity downstream enzymes. Furthermore, overexpression lentivirus transfection partially prevented These demonstrated induces dysfunction acts as an endogenous protective factor ototoxicity.